Relationships between cardiovascular remodelling and the pulse pressure in never treated hypertension

Jp, Baguet; Jm, Mallion; Moreau–Gaudry, Alexandre; Noirclerc, M; Péoc’h, Michel; Jp, Siché

doi:10.1038/sj.jhh.1000933

Cited by 37 publications

(17 citation statements)

References 43 publications

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“…These investigations were performed with a methodology previously described in detail. 10,11 Urinary 15-F 2t -IsoP Measurements Urine samples (20 mL) were collected between 8 and 10 AM in polyethylene tubes, immediately refrigerated and transferred to the laboratory, aliquoted, and stored at Ϫ20°C. Urinary levels of 15-F 2t -IsoP were measured using gas chromatography/mass spectrometry as previously described.…”

Section: Methodsmentioning

confidence: 99%

Lipid Peroxidation Is Not Increased in Patients With Untreated Mild-to-Moderate Hypertension

et al. 2003

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Abstract-In contrast with the huge amount of experimental data available, only few and somewhat unconvincing clinical studies support the hypothesis that oxidative stress is involved in the early stages of essential hypertension in humans. Isoprostanes are chemically stable lipid peroxidation products of arachidonic acid, the quantification of which provides a novel approach to the assessment of oxidative stress in vivo. The main objective of this study was to quantify the urinary levels of 15-F 2t -IsoP in the early stages of essential hypertension, using gas chromatography/mass spectrometry, by comparing 30 patients with never-treated mild-to-moderate hypertension with 30 gender-and age-paired healthy controls. Urinary 15-F 2t -IsoP levels were not significantly different in hypertensive patients (69Ϯ36 pmol/mmol creatinine) compared with controls (75Ϯ34 pmol/mmol creatinine, 95% confidence intervals on differences: Ϫ23 to 13). No significant correlation was found between basal urinary 15-F 2t -IsoP levels and age, low-density lipoprotein cholesterol, glucose, clinical pulse pressure, carotid intima-media thickness, left ventricular mass index, or aortic pulse wave velocity.In conclusion, this study shows that lipid peroxidation is not increased in never-treated mild-to-moderate hypertension. This suggests that oxidative stress is not implicated in the pathogenesis of human essential hypertension, at least in the early stages.

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Section: Methodsmentioning

confidence: 99%

Lipid Peroxidation Is Not Increased in Patients With Untreated Mild-to-Moderate Hypertension

et al. 2003

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“…28,29) The increase in PP is an age-related phenomenon 28) and an indicator of large artery stiffness 29) ; this last condition increases afterload 30) and myocardial oxygen demand, impairs ventricular relaxation, and causes subendocardial ischemia even in the absence of CAD. 31) These effects make elderly people more prone to myocardial ischemia and ventricular dysfunction (ie. to CHF).…”

Section: )mentioning

confidence: 99%

Predictors of Congestive Heart Failure Mortality in Elderly People From the General Population The CArdiovascular STudy in the ELderly (CASTEL)

et al. 2005

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SUMMARYCongestive heart failure (CHF) is highly prevalent in the elderly. The aim of this study was to identify the predictors of CHF mortality in patients over 65 years of age who were free of CHF at initial screening. A total of 3,282 elderly subjects were recruited in a population-based frame and 12-year events were recorded. Continuous items were divided into tertiles and for each tertile adjusted the relative risk (RR) with 95% confidence intervals (CI) was derived in both genders from multivariate Cox analysis of CHF mortality.Age

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“…2,3 Pulse pressure (PP), a marker of the stiffness of large arteries, 4 has recently emerged as an important risk marker, and several studies have documented an association between increased PP and left ventricular hypertrophy (LVH). [5][6][7] Although the pathogenesis of LVH in hypertensive humans is quite complex due to the concurrent contribution of several haemodynamic and nonhaemodynamic factors, 2 it is still uncertain which of the different BP components exerts the prevalent influence on the pathogenesis of LVH and its regression in hypertensive humans.…”

Section: Introductionmentioning

confidence: 99%

Does the reduction in systolic blood pressure alone explain the regression of left ventricular hypertrophy?

Verdecchia¹,

Angeli²,

Gattobigio

et al. 2004

J Hum Hypertens

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Systolic blood pressure (SBP) is an important determinant of the development and regression of left ventricular hypertrophy (LVH) in hypertensive humans. However, comparative assessments with other BP components are scarce and generally limited in size. As part of the Progetto Ipertensione Umbria Monitoraggio Ambulatoriale (PIUMA), 743 hypertensive subjects underwent echocardiography and 24-h ambulatory BP monitoring before and after an average of 3.9 years of treatment. The changes in left ventricular mass showed a significant direct association with the changes in 24-h SBP (r ¼ 0.40), diastolic blood pressure (DBP) (r ¼ 0.33) and pulse pressure (PP) (r ¼ 0.35). Weaker associations were found with the changes in clinic BP (r ¼ 0.32, 0.31 and 0.16, respectively). In a multivariate linear regression analysis, the changes in 24-h SBP were the sole independent determinants of the changes in left ventricular mass (LVM) according to the following equation: percentage changes in LVM ¼ 0.73 Â (percentage changes in 24-h SBP) À0.48 (Po0.0001). For any given reduction in 24-h SBP, the reduction in LVM did not show any association with the changes in DBP and PP, either clinic or ambulatory. These data indicate that SBP is the principal determinant of LVH regression in hypertensive humans.

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Relationships between cardiovascular remodelling and the pulse pressure in never treated hypertension

Cited by 37 publications

References 43 publications

Lipid Peroxidation Is Not Increased in Patients With Untreated Mild-to-Moderate Hypertension

Lipid Peroxidation Is Not Increased in Patients With Untreated Mild-to-Moderate Hypertension

Predictors of Congestive Heart Failure Mortality in Elderly People From the General Population The CArdiovascular STudy in the ELderly (CASTEL)

Does the reduction in systolic blood pressure alone explain the regression of left ventricular hypertrophy?

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